Kelch-like ECH-associated protein (Keap1)-nuclear factor erythroid-2-related factor 2 (Nrf2) protein-protein interaction has become an important drug target for the treatment of Alzheimer's disease. In this study, we found a novel piperine derivative (HJ22) synthesized by our group with great ability to bind to Keap-1 and activate Keap1-Nrf2-ARE signaling pathway in vitro, driving us to investigate the beneficial effects of HJ22 on ibotenic acid (IBO)-induced neurological disorders in rats and underlying mechanisms. Interestingly, HJ22 significantly ameliorated IBO-induced cognitive impairment in Morris water maze, Y-maze and passive avoidance tests. Moreover, HJ22 significantly attenuated cholinergic dysfunction and neuronal morphological changes via inhibiting apoptotic cell death induced by IBO. Notably, HJ22 inhibited the interaction between Keap1 and Nrf2, and subsequently up-regulated nuclear Nrf2 expression, thereby inhibiting oxidative stress and Thioredoxin-interacting protein (TXNIP)-mediated Nod-like receptor protein 3 (NLRP3) inflammasome activation. These findings demonstrated that HJ22 exhibited potent therapeutic effects against IBO-induced cognitive impairment by alleviating cholinergic damage, oxidative stress, apoptosis and neuroinflammation, which might be partly attributed to its inhibitory activity on Keap1-Nrf2 protein-protein interaction. Vascular inflammation plays a decisive role in the formation of foam cells and in the pathophysiology of atherosclerosis. However, the underlying mechanisms of these processes are not clearly understood. Macrophages engulf oxidized low-density lipoproteins (OxLDLs) via a scavenger receptor (SR), an event that mediates the elaboration of proinflammatory cytokines to initiate necrotic core formation in atherogenic plaques. In this study, we demonstrate that Nitric oxide synthase 1 (NOS1)-derived nitric oxide (NO) promotes OxLDL uptake and enhances the release of proinflammatory cytokines by macrophages. Conversely, we show that NOS1 inhibition by N(G)-nitro-L-arginine methyl ester (L-NAME) suppresses OxLDL uptake and proinflammatory cytokine expression. Current studies indicate that NOS1 plays a crucial role in vascular inflammation and in the progression of atherosclerosis. Therefore, interference with NOS1 enzymatic activity should serve as an effective strategy to reduce foam cell formation and limit the extent of atherosclerotic plaque expansion. Selenium can alleviate the inflammatory reaction infected by Staphylococcus aureus (S. aureus). However, the role of selenium on the autophagy in RAW264.7 macrophages infected by S. aureus has not been reported. The goal of this study was to clarify the effect of selenium on the autophagy and related inflammatory pathways (MAPK and NF-κB) in RAW264.7 macrophages infected by S. aureus. RAW264.7 macrophages were co-treated with Na2SeO3 and S. aureus. The expression of related inflammatory pathways (MAPK and NF-κB) and autophagy-related proteins were detected by Western blotting. The microtubule-binding protein light chain 3 (LC3) puncta were measured with immunofluorescence staining. https://www.selleckchem.com/products/3-3-cgamp.html The ultrastructure of RAW264.7 macrophages infected by S. aureus was detected by transmission electron microscope (TEM). And plate counting method was used to detect the proliferation of S. aureus in RAW264.7 macrophages. The results showed that the expression levels of LC3 II increased and the expression levels of p62 decreased after adding selenium, compared with S. aureus infection group. Compared with S. aureus infection group, the intracellular LC3 puncta and autophagic vesicles, autophagosomes, and autolysosomes increased with selenium supplementation. The number of S. aureus proliferation decreased with addition of selenium, compared with S. aureus infection group. Selenium could significantly inhibit the phosphorylation of MAPK and NF-κB signaling pathway key proteins, compared with S. aureus infection group. In summary, selenium could promote the autophagy in macrophages infected by S. aureus, alleviate the blockade of autophagic flow, depress the transcription of MAPK and NF-κB signaling pathways, and inhibit the proliferation of S. aureus in RAW264.7 macrophages. PURPOSE Epilepsy in adolescents affects their psychological health, independence, and emotional adjustment. Psychological and self-management interventions might give benefits to adolescent with epilepsy in terms of quality of life, emotional well-being, and reduced fatigue. "Fondazione Tender To Nave Italia" promotes a project using sailing activities as an empowerment opportunity. The main aim of our study was to examine the empowerment effects on quality of life of adolescents with epilepsy attending sailing activities, and to compare the results perceived by adolescents and their parents. METHODS Fifty-eight patients with a diagnosis of epilepsy were included in an empowerment project titled "Waves rather than spikes" from June 2013 to July 2018. Intellectual level was based on the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) criteria. Patients were administered Pediatric Quality of Life Inventory (PedsQL), adolescent and parent version. Behavioral data were collected by parer to reduce the burden of epilepsy in adolescents, and to improve quality of life. These are critical factors for a well-managed transition phase to adulthood. The evaluation of the role of anomalous neuronal networks in epilepsy using a graph theoretical approach is of growing research interest. There is currently no consensus on optimal methods for performing network analysis, and it is possible that variations in study methodology account for diverging findings. This review focuses on global functional and structural interictal network characteristics in people with idiopathic generalized epilepsy (IGE) with the aim of appraising the methodological approaches used and assessing for meaningful consensus. Thirteen studies were included in the review. Data were heterogenous and not suitable for meta-analysis. Overall, there is a suggestion that the cerebral neuronal networks of people with IGE have different global structural and functional characteristics to people without epilepsy. However, the nature of the aberrations is inconsistent with some studies demonstrating a more regular network configuration in IGE, and some, a more random topology. There is greater consistency when different data modalities and connectivity subtypes are compared separately, with a tendency towards increased small-worldness of networks in functional electroencephalography/magnetoencephalography (EEG/MEG) studies and decreased small-worldness of networks in structural studies.